Intracranial hypertension develops from the initial cerebral effect of increased intracranial pressure and becomes symptomatical; then it acquires its individuality, surpassing the initial disease. The intracranial hypertension syndrome corresponds to the stage at which the increases in intracranial pressure (ICP) can be compensated and the ICH disease is in its acute form, equivalent to a decompensated ICH syndrome. Based on the etiopathogenesis of intracranial hypertension, a new classification is proposed: parenchymatous intracranial hypertension with an intrinsic cerebral cause; vascular intracranial hypertension, which has its etiology in disorders of the cerebral blood circulation; and essential or idiopathic intracranial hypertension, the former pseudotumor cerebri, an incomplete ICH syndrome. A synergetical pattern of the ICH is based on the relation between ICP and the period of high-pressure action: the critical pressure–time fluctuation causes the autoregulation of the cerebral blood flow to decrease or determines the brain herniation. The decompensation is a state of instability and appears when the intrinsic ratio of pressure–time fluctuation is changed: the high ICP lasts longer than the corresponding normal ICP, or the ICP is higher than the one that normally lasts the same period of time.

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